Ethology Of Tumors Flashcards
Areca nut causes….
Oral submucous fibrosis
Human t cell leukemia virus…
Causes acute tcell leukemia
EBV causes …
Nasopharyngeal carcinoma and burkitt lymphoma
Low intake of vit …. cause cancer
C E A
Non intervention for premalignant lesions (mild to mod)
Patient reviewed
regularly every 3-6 months and examined clinically for any changes
in lesion that would require any further
biopsy. If the lesion
appears clinically unchanged. It should still be necessary to perform a repeat biopsy no longer than 3
years after the initial
biopsy.
Follow up for cancer surgery patiens
All patients must be placed on life-long review of about 6 monthly intervals.
Premalignant lesions also include
- SLE 🦋
- white lesions associated with smokeless tobacco
- solar chelitis 🌞
Clinical appearance of leukoplakia?
Homogenous leukoplakia Usually plaque like, but some
variations surface may e present: May be smooth or wrinkled or the surface is criss-crossed by small cracks or fissures producing a tessellated appearance.
Non-homogenous leukoplakia
Surface may show ulceration or nodular
thickening causing a warty appearance so called verrucous leukoplakia or area of redness due to association with erythroplakia so called speckled leukoplakia.
Histo of leukoplakia
H/P(pathology of epithelial dysplasia): ✓ Wide range in H/P from keratosis to epithelial dysplasia.
The term leukoplakia has no specific histopathological
connotation, but is a clinical diagnosis after exclusion of
other diseases (not based on any H/P features).
✓ H/P show:
- Varying degrees of keratosis,
- Changes in epithelial thickness.
- Epithelial dysplasia (may be).
- Varying degrees of chronic inflammatory cells infiltration in lamina propria (CT).
Signes of dysplasia you forget often
(3) Prominent nucleoli.
4. (1) in nuclear/cytoplasmic ratio.
5. Abnormal mitosis may be: (15 Increased in number.
Abnormal form as tri-radiate mitosis.
Site higher than usual (away from basal and
supra-basal mitosis).
7 Loss of polarity of basal cell layer (loss of cellular orientation) → the basal cells have no definite long axis & nuclei have no regular polarity.
9 Abnormal keratinization beneath the normal keratin layer either
as:
Individual cell keratinization within stratum spinosum (prickle). Disturbed maturation of group of cells formation of
intraepithelial keratin pearls.
Loss or of intercellular cohesion. Irregular epithelial stratification →→ abnormal thickness of
epithelium (area is more thin than other area). → Cells don’t show proper sequence of morphological and
maturational changes from basal cell layer to surface.
Carcinoma in situ does it have keratin
With or without thin layer of parakeratin on the surface.
Histology of erythroplakia
It may show either moderate epithelial dysplasia or carcinoma in situ or superficially
invasive sq.c.c.
o Keratin production. o Epithelium:
✓ Atrophic→ allow the underlying blood vessels to show through red color. ✓May be hyperplastic in some areas.
o Chronic inflammatory cells infiltration of CT.
Erythroplakia clinical
Age, sex x-old males,
2 Common sites →→ floor of mouth, tongue, soft palate.
3 Asymptomatic, may be multiple, well demarcated erythematous macule or
plaque with soft, velvety texture. 4. May be homogenous or non-homogenous.
Clinical features of oral submucous fibrosis
-young adults with areca nut consumption and betel leaf
-1st signes
Petechia
Vesicles
Mucosal burns
Xerostomia
- then
Marble like palor
Trismus
Mucosal pain with spicy food 🌶
-If 👅
Small immobile and devoid of papilla
-happens in retromolar area of cheek and soft palate
Natue of oral submucous fibrosis
Progressive chronic highly premalignant
